Unraveling new mechanisms of exercise intolerance in chronic heart failure. Role of exercise training

2012 ◽  
Vol 18 (1) ◽  
pp. 65-77 ◽  
Author(s):  
Viviane M. Conraads ◽  
Emeline M. Van Craenenbroeck ◽  
Catherine De Maeyer ◽  
An M. Van Berendoncks ◽  
Paul J. Beckers ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Exercise Training ◽  
Exercise Intolerance

scholarly journals Clinical Utility of Exercise Training in Heart Failure with Reduced and Preserved Ejection Fraction

2015 ◽  
Vol 9 ◽  
pp. CMC.S21372 ◽  
Author(s):  
Muhammad Asrar Ul Haq ◽  
Cheng Yee Goh ◽  
Itamar Levinger ◽  
Chiew Wong ◽  
David L. Hare
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Ejection Fraction ◽  
Exercise Tolerance ◽  
Exercise Intolerance ◽  
Sufficient Evidence ◽  
Preserved Ejection Fraction ◽  
Reduced Ejection Fraction ◽  
Patients With Heart Failure

Reduced exercise tolerance is an independent predictor of hospital readmission and mortality in patients with heart failure (HF). Exercise training for HF patients is well established as an adjunct therapy, and there is sufficient evidence to support the favorable role of exercise training programs for HF patients over and above the optimal medical therapy. Some of the documented benefits include improved functional capacity, quality of life (QoL), fatigue, and dyspnea. Major trials to assess exercise training in HF have, however, focused on heart failure with reduced ejection fraction (HFREF). At least half of the patients presenting with HF have heart failure with preserved ejection fraction (HFPEF) and experience similar symptoms of exercise intolerance, dyspnea, and early fatigue, and similar mortality risk and rehospitalization rates. The role of exercise training in the management of HFPEF remains less clear. This article provides a brief overview of pathophysiology of reduced exercise tolerance in HFREF and heart failure with preserved ejection fraction (HFPEF), and summarizes the evidence and mechanisms by which exercise training can improve symptoms and HF. Clinical and practical aspects of exercise training prescription are also discussed.

scholarly journals Exercise intolerance in patients with chronic heart failure: role of impaired nutritive flow to skeletal muscle.

Circulation ◽  
1984 ◽  
Vol 69 (6) ◽  
pp. 1079-1087 ◽  
Author(s):  
J R Wilson ◽  
J L Martin ◽  
D Schwartz ◽  
N Ferraro
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Exercise Intolerance

scholarly journals Exercise training in chronic heart failure: improving skeletal muscle O2transport and utilization

2015 ◽  
Vol 309 (9) ◽  
pp. H1419-H1439 ◽  
Author(s):  
Daniel M. Hirai ◽  
Timothy I. Musch ◽  
David C. Poole
Keyword(s):  
Quality Of Life ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Exercise Training ◽  
Physical Capacity ◽  
Exercise Intolerance ◽  
Whole Body ◽  
Functional Components

Chronic heart failure (CHF) impairs critical structural and functional components of the O2transport pathway resulting in exercise intolerance and, consequently, reduced quality of life. In contrast, exercise training is capable of combating many of the CHF-induced impairments and enhancing the matching between skeletal muscle O2delivery and utilization ( Q̇mO2and V̇mO2, respectively). The Q̇mO2/ V̇mO2ratio determines the microvascular O2partial pressure (PmvO2), which represents the ultimate force driving blood-myocyte O2flux (see Fig. 1). Improvements in perfusive and diffusive O2conductances are essential to support faster rates of oxidative phosphorylation (reflected as faster V̇mO2kinetics during transitions in metabolic demand) and reduce the reliance on anaerobic glycolysis and utilization of finite energy sources (thus lowering the magnitude of the O2deficit) in trained CHF muscle. These adaptations contribute to attenuated muscle metabolic perturbations (e.g., changes in [PCr], [Cr], [ADP], and pH) and improved physical capacity (i.e., elevated critical power and maximal V̇mO2). Preservation of such plasticity in response to exercise training is crucial considering the dominant role of skeletal muscle dysfunction in the pathophysiology and increased morbidity/mortality of the CHF patient. This brief review focuses on the mechanistic bases for improved Q̇mO2/ V̇mO2matching (and enhanced PmvO2) with exercise training in CHF with both preserved and reduced ejection fraction (HFpEF and HFrEF, respectively). Specifically, O2convection within the skeletal muscle microcirculation, O2diffusion from the red blood cell to the mitochondria, and muscle metabolic control are particularly susceptive to exercise training adaptations in CHF. Alternatives to traditional whole body endurance exercise training programs such as small muscle mass and inspiratory muscle training, pharmacological treatment (e.g., sildenafil and pentoxifylline), and dietary nitrate supplementation are also presented in light of their therapeutic potential. Adaptations within the skeletal muscle O2transport and utilization system underlie improvements in physical capacity and quality of life in CHF and thus take center stage in the therapeutic management of these patients.

scholarly journals The role of exercise training in chronic heart failure

Heart ◽  
1997 ◽  
Vol 78 (5) ◽  
pp. 431-436 ◽  
Author(s):  
R. P Wielenga ◽  
A. J S Coats ◽  
W. L Mosterd ◽  
I. A Huisveld
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Exercise Training

Role of endothelin in the exercise intolerance of chronic heart failure

1995 ◽  
Vol 75 (17) ◽  
pp. 1282-1283 ◽  
Author(s):  
Henry Krum ◽  
Rochelle Goldsmith ◽  
Michelle Wilshire-Clement ◽  
Myron Miller ◽  
Milton Packer
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Exercise Intolerance

Exercise Intolerance in Chronic Heart Failure: The Role of Cortisol and the Catabolic State

2013 ◽  
Vol 11 (1) ◽  
pp. 70-79 ◽  
Author(s):  
Georgios Tzanis ◽  
Stavros Dimopoulos ◽  
Varvara Agapitou ◽  
Serafim Nanas
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Exercise Intolerance ◽  
Catabolic State

scholarly journals Exercise intolerance and fatigue in chronic heart failure: is there a role for group III/IV afferent feedback?

2020 ◽  
Vol 27 (17) ◽  
pp. 1862-1872
Author(s):  
Luca Angius ◽  
Antonio Crisafulli
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Potential Role ◽  
Muscle Afferents ◽  
Afferent Feedback ◽  
Exercise Intolerance ◽  
Peripheral Fatigue ◽  
Group Iii ◽  
Exercise Induced

Exercise intolerance and early fatiguability are hallmark symptoms of chronic heart failure. While the malfunction of the heart is certainly the leading cause of chronic heart failure, the patho-physiological mechanisms of exercise intolerance in these patients are more complex, multifactorial and only partially understood. Some evidence points towards a potential role of an exaggerated afferent feedback from group III/IV muscle afferents in the genesis of these symptoms. Overactivity of feedback from these muscle afferents may cause exercise intolerance with a double action: by inducing cardiovascular dysregulation, by reducing motor output and by facilitating the development of central and peripheral fatigue during exercise. Importantly, physical inactivity appears to affect the progression of the syndrome negatively, while physical training can partially counteract this condition. In the present review, the role played by group III/IV afferent feedback in cardiovascular regulation during exercise and exercise-induced muscle fatigue of healthy people and their potential role in inducing exercise intolerance in chronic heart failure patients will be summarised.

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